10 Polka Dot/Thinkstock Images.com/Corbis Regulation of Sexual Behavior Learning Objectives After completing this chapter, you should be able to: • • • • • • • Describe the process by which we become biological males and biological females. Explain the role of chromosomes and hormones in sexual differentiation. Name five different developmental disorders associated with missing or extra chromosomes or hormones. Identify differences between the male and female brain. Draw a graph that shows the changes in hormone levels in women throughout their menstrual cycles. List at least five sexual disorders in women. Explain the role of hormones in the maturation of the male reproductive system. wiL81028_10_c10_301-326.indd 301 7/10/13 12:31 PM Section 10.1 Sexual Differentiation CHAPTER 10 Molly is a girl who was born a boy. That is, she possesses the sex chromosomes of a male (one X and one Y chromosome), and she was born with testes and a scrotum. However, she was born without a penis, a rare defect known as cloacal exstrophy. Her surprised and dismayed parents elected for Molly to have reconstructive surgery that involved removing the testes and giving Molly the appearance of having female external genitalia. And Molly was raised a girl. She was dressed in girls’ clothing, given girls’ toys to play with, and socialized to be a girl. However, she was always a bit different, compared to other girls. She preferred the rough-and-tumble games of boys. In fact, she preferred playing with boys. By the time Molly reached puberty, she felt more like a boy than a girl, despite her family’s attempts to raise her as a girl. Molly’s story is similar to the stories of many children whose parents elected to raise them in a gender role that is not consistent with their biological sex. In a recent study, 14 out of 25 children who were reassigned sex at birth feel that they are the wrong sex (Reiner, Gearhart, & Jeffs, 1999). That is, in most cases biological boys who have been raised as girls feel like boys. This suggests that sex hormones affect the development of the brain before birth, making an indelible impression on the fetus that cannot be taken away by a surgeon’s knife. In this chapter we will look at how sex hormones affect behavior. We will examine their influence on physical development, perceptual ability, and sexual behavior. 10.1 Sexual Differentiation S exual differentiation, the process by which we become biological males or females, begins at conception. A female embryo develops when a sperm cell bearing an X chromosome and an egg or ovum, which always carries an X chromosome, are united. On the other hand, a male embryo develops when a sperm bearing a Y chromosome fertilizes an ovum. Recall from Chapter 2 that the Y chromosome is much smaller than the X chromosome and contains relatively little genetic material. In fact, the Y chromosome appears to have one function: to direct the development of the testes. The embryo has the ability to develop into a male or a female. We all start out with the same equipment that is capable of taking a male or female form. The developing embryo has two primordial gonads (Figure 10.1). In an embryo with a Y chromosome, the Y chromosome directs the primordial gonads to develop into male gonads, or testes (Arnold, Chen, & Itoh, 2012). (Testis is the singular of testes.) wiL81028_10_c10_301-326.indd 302 7/10/13 12:31 PM CHAPTER 10 Section 10.1 Sexual Differentiation Figure 10.1: Sexual differentiation Sexual differentiation depends on whether the sperm was carrying an X or Y chromosome when it reached the ovum. Sexual appearance of baby at second to third month of pregnancy Genital tubercule Urethrolabial fold Genital groove Labioscrotal swelling Anus Female and male identical Sexual appearance of baby at third to fourth month of pregnancy Sexual appearance of baby at time of birth Genital tubercule Inner labial fold Vulval groove Anus Clitoris Labia majora Labia minora Anus Outer labial swelling Opening of urethra Opening of vagina Genital tubercule Urethral groove Anus Penis Scrotum Urethral fold Scrotal swelling Joining line of urethral fold Joining line of scrotal swellings Anus In the absence of the Y chromosome, the female reproductive system develops. The primordial gonad develops into the female gonad or ovary, when the Y chromosome is missing. The ovary can be characterized as the default gonad because it emerges if the Y chromosome is absent. wiL81028_10_c10_301-326.indd 303 7/10/13 12:32 PM Section 10.1 Sexual Differentiation CHAPTER 10 Organizational Effects of Hormones The gonads produce hormones, called gonadal hormones, which direct the development of the internal genitalia and external genitalia. During embryonic development, gonadal hormones have organizational effects, which are permanent and cannot be reversed. That is, gonadal hormones influence the development of the reproductive system and the nervous system (MacLusky & Naftolin, 1981). As soon as the testes develop, they begin to produce a hormone called testosterone. Testosterone is released into the bloodstream, where it travels to other parts of the body, including the brain. The developing brain is especially vulnerable to the effects of testosterone, which alters the formation of the hypothalamus, the cerebrum, and other areas, as you will learn later in this chapter. Testosterone also affects the development of the internal genitalia and external genitalia. Internal Genitalia Male internal genitalia are located inside the male’s abdomen and include the vas deferens, epididymis, and associated glands, such as the prostate gland. In the female body, internal genitalia include the vagina, uterus, and fallopian tubes. However, in the earliest embryonic stages, male and female alike have the ability to develop male or female internal genitalia. This is because embryos possess two sets of internal organs, called the Wolffian and the Mullerian ducts. The Wolffian ducts are the precursors of the male internal genitalia. Under the influence of testosterone, the Wolffian ducts flourish and develop into the internal plumbing of the normal male reproductive system. The testes also secrete another hormone known as Mullerian inhibiting substance. This hormone does exactly what its name implies: It inhibits the development of the Mullerian ducts, which means that the vagina, uterus, and fallopian tubes do not develop in the male body. Thus, the testicular hormones, testosterone and Mullerian inhibiting substance, orchestrate the development of the male internal reproductive system by stimulating the growth of the Wolffian system and preventing the growth of the Mullerian ducts. Female internal genitalia, which arise from the Mullerian system, are the default structures that develop when testes and testicular hormones are absent. Because the ovaries develop in the female body, no Mullerian inhibiting substance is produced. In addition, the ovaries produce ovarian gonadal hormones, including estrogen and progesterone, which are believed to inhibit the action of testosterone in the female body (Novy & Resko, 1981). This means that the Wolffian ducts do not develop, because they require testosterone for their development, and thus they wither away. The Mullerian ducts, however, flourish and grow because there is no Mullerian inhibiting substance to prevent their development. Therefore, the vagina, uterus, and fallopian tubes grow and mature in the female body due to the absence of testosterone and Mullerian inhibiting substance. External Genitalia The final form of the external genitalia is also determined by the presence of testosterone. In its earliest stages, the embryo possesses a unisex external appearance. Both male and female embryos have protruding tufts of flesh called the genital tubercle, urethrogenital folds, and labioscrotal swellings (Figure 10.1). In the male’s body, testosterone is converted to dihydrotestosterone, which in turn changes the external appearance of the embryonic genitalia. The presence of wiL81028_10_c10_301-326.indd 304 7/10/13 12:32 PM Section 10.1 Sexual Differentiation CHAPTER 10 dihydrotestosterone causes the genital tubercle to transform into the glans (or head) of the penis, the urethrogenital folds to close up to form the body of the penis, and the labioscrotal swelling to become the scrotum that holds the testes. The testes actually descend into the scrotum later in development. In contrast, the external genitalia become female when dihydrotestosterone is not present. The genital tubercle transforms into the clitoris, the urethrogenital folds become the labia minora, and the labioscrotal swellings develop into the labia majora, in the absence of testosterone (Figure 10.1). The female reproductive system can be characterized as the default system: The body takes a female form if the Y chromosome or testicular hormones are missing, as you will learn in the next section. Variations in Sexual Differentiation For most individuals, sexual differentiation goes smoothly, and the body’s sexual appearance at birth is normal and appropriate for their chromosomal designation. However, some people develop abnormally due to genetic variations or exposure to hormone-like chemicals in the mother’s uterus (Hiort, 2000; Hiort & Holterhus, 2000). In this section we will consider a number of syndromes that alter sexual differentiation. Genetic Variations Human beings typically have 46 chromosomes, 22 pairs of autosomal chromosomes and 1 pair of sex chromosomes, as you learned in Chapter 2. Human males normally have the chromosomal designation 46, XY, whereas human females normally have the chromosomal designation 46, XX. It is important to keep in mind that not all people have 46 chromosomes. For example, some individuals have fewer than 46 chromosomes, as in the case of people with Turner’s syndrome; they are missing a sex chromosome and have a chromosomal designation of 45, XO. Because these individuals lack a Y chromosome, they do not develop testes and therefore do not produce testosterone or Mullerian inhibiting substance. This means that individuals with Turner’s syndrome have the “default body,” with female internal and external genitalia. However, because they are missing a sex chromosome, individuals with Turner’s syndrome have a sterile female gonad or ovary and cannot become pregnant. These individuals are raised as girls and develop with a female gender identity. They are typically short in stature and often have a short neck or a neck with a webbed appearance. In contrast, individuals with Klinefelter’s syndrome have the chromosomal designation 47, XXY. That is, they have an extra sex chromosome. People with Klinefelter’s syndrome have functional testes, because they possess a Y chromosome, and therefore have typical male internal and external genitalia, although sometimes they have a penis that is smaller than normal. Keep in mind that the presence or absence of a Y chromosome determines whether or not testes will develop and whether or not testosterone will be produced. Whether a person has a chromosomal designation of XY, XXXY, or XXXXXY, the presence of a Y chromosome dictates that testes will develop and, as a consequence, that male internal and external genitalia will form. Individuals with a 45, YO chromosomal designation (an unpaired Y chromosome) have not been identified. Having an unpaired Y chromosome most likely results in miscarriage or embryonic death (Weekes, 1994). wiL81028_10_c10_301-326.indd 305 7/10/13 12:32 PM Section 10.1 Sexual Differentiation CHAPTER 10 Some individuals, referred to as true hermaphrodites, are born with both ovarian and testicular tissue. Typically, true hermaphrodites have a chromosomal designation of 46, XX. However, a fragment of the Y chromosome that directs the growth of testes is found on another chromosome in true hermaphrodites (Kojima et al., 1998; Margarit et al., 2000). This means that, although hermaphroditic individuals do not actually have a Y chromosome, they inherit a fragment of the Y chromosome from one parent, which causes one or more testes to be produced. Testosterone is produced by the testis and released into the bloodstream, where it promotes the growth of male internal and external genitalia. Mullerian inhibiting substance may or may not be produced, and thus the individual may or may not develop female internal genitalia. At puberty, estrogen produced by the ovary will stimulate the growth of breasts and curvature of the hips. If female internal genitalia are present, menstruation will begin. Because true hermaphrodites are usually born with a penis or a structure resembling a phallus, they are typically raised as boys, even if a vagina is also present. In this case surgical removal of the ovaries and other female organs is performed to enable the adoption of a male gender identity. On the other hand, when no phallus is present, a female gender assignment is usually given. Typically, the parents make gender assignments shortly after the individual’s birth. A number of investigators have questioned the appropriateness of gender assignment by the parents before the individual is able to choose the gender that is most comfortable for them (Fausto-Sterling, 1999; Kuhnle & Krahl, 2002; Nussbaum, 2000). Some genetic variations leading to faulty sexual differentiation are not due to the absence of a sex chromosome or to the presence of an extra sex chromosome. Instead, they are due to a mutation on an autosome. For example, some biological males with a chromosomal designation of 46, XY are born with female external genitalia. These males have a genetic mutation that causes a deficiency of the enzyme that prevents the conversion of testosterone to dihydrotestosterone (Cai et al., 1996). Recall that testosterone is capable of stimulating growth of the Wolffian system, but it cannot stimulate development of the penis and scrotum. Thus, these boys are born with male internal genitalia and female external genitalia. At puberty, however, the surge in hormonal release from the testes produces enough testosterone to stimulate the growth of the penis. To the amazement of the affected individual and family, the girl transforms into a boy as the penis grows, the testes descend into the scrotum, and secondary sex characteristics associated with the male body develop. This condition is nicknamed guevedoces, or “eggs (testes) at twelve” (gueve- means “eggs” and -doces means “twelve” in Spanish). Although these individuals are raised as girls, they readily adopt a male gender identity, dressing and acting like men, after they develop male external genitalia (Imperato-McGinley, Guerrero, Gautier, & Peterson, 1974). Testosterone was present during brain development in these individuals, which may contribute to the adoption of a male sex role. Some individuals with this disorder do not adjust well to their life as a man, however (Aartsen, Gallee, Snethlage, & Van Geel, 1994). Another genetic mutation leads to a disorder known as androgen insensitivity syndrome. The word androgen refers to all male hormones, including testosterone. Individuals with this disorder have the chromosomal designation 46, XY. However, they are insensitive to the testosterone produced by their own testes. That is, because they have a Y chromosome, testes develop. The testes secrete testosterone and Mullerian inhibiting substance. The Mullerian inhibiting substance prevents the growth of the Mullerian system, which means that they do not develop a uterus or vagina. In addition, the individual’s insensitivity or inability to respond to testosterone prevents the development of the Wolffian system. Thus, the individual with androgen insensitivity syndrome has neither male nor female internal genitalia. The external genitalia, however, take the default female form because the individual’s body cannot respond to testosterone and acts as if no testosterone is present. When the child is born, it appears to be a girl and is raised female. wiL81028_10_c10_301-326.indd 306 7/10/13 12:32 PM Section 10.1 Sexual Differentiation CHAPTER 10 For many individuals with androgen insensitivity syndrome, no problem is noticed until puberty. At the time of puberty, these individuals may develop breasts due to the increased release of estrogen from the adrenal gland, but menstruation does not occur. A gynecological exam quickly reveals the problem: Undescended testes are found in the abdominal cavity, but no uterus or ovaries are found. Because such individuals are insensitive to testosterone and other androgens, hormone therapy cannot transform a woman with androgen insensitive syndrome into a man, even though she has a Y chromosome. Indeed, because the individual has been raised female and because testosterone has not affected the development of her nervous system, she is typically comfortable in that gender role and is happy to remain a woman. Estrogen hormone treatments stimulate the growth of breasts and other female secondary sex characteristics, although the affected woman will never be able to get pregnant because she lacks ovaries and a uterus. The “Case Study” describes the case of a young woman with androgen insensitivity syndrome (Hughes et al., 2012). Case Study: Androgen Insensitivity Syndrome Carolyn was a college freshman with an embarrassing problem. She had no vagina. When she was 14, her mother took her to her gynecologist because she was worried that her daughter had not begun menstruating and showed few signs of sexual maturation. Because of Carolyn’s youth, the female gynecologist performed a pelvic exam by inserting a finger into Carolyn’s rectum. The gynecologist could not locate a uterus in Carolyn’s pelvis, but she did find two firm, egg-shaped structures that she knew were not ovaries. An ultrasound test and blood tests were ordered for Carolyn. The ultrasound confirmed the absence of a uterus and the presence of two testes in Carolyn’s pelvic cavity. The blood tests showed high levels of testosterone and very low levels of estrogen in her blood. What’s more, a chromosome test indicated that Carolyn had both X and Y chromosomes in each cell of her body. Very gently, the gynecologist told Carolyn and her mother that Carolyn had a rare disorder called androgen insensitivity syndrome. The doctor explained that Carolyn would never be able to have a baby because she had no uterus or ovaries. Carolyn didn’t understand much of what the doctor told her. At 14 years of age, Carolyn was not thinking about having babies. But she began to worry that nobody would marry her because she couldn’t have babies. The physician also told Carolyn that she had no vagina, but that she could have a vagina surgically constructed when she was older. Carolyn asked if doctors couldn’t also construct a uterus for her so that she could have babies. The doctor laughed softly, shook her head, and, using diagrams in a book, explained to Carolyn why only a vagina could be replaced. Carolyn blushed when the doctor showed her the pictures of women’s bodies, and she didn’t like talking about embarrassingly intimate parts of her body. The gynecologist asked for a family history because androgen insensitivity syndrome is so rare. Carolyn’s father had married the daughter of his first cousin, which meant that Carolyn and her mother shared one set of great-grandparents. Although the physician couldn’t say for certain whether that was why Carolyn had her unusual disorder, she assured Carolyn and her mother that most people with Carolyn’s disorder did not have close intermarriages in their families. Carolyn was placed on estrogen therapy, which caused her pubic hair and breasts to grow. Tall and lanky, she developed into a very attractive and feminine young woman. In high school she had a series of boyfriends and felt sexually attracted to them. However, she avoided sexual contact with them because she feared that they would discover that she was “different.” (continued) wiL81028_10_c10_301-326.indd 307 7/10/13 12:32 PM Section 10.1 Sexual Differentiation CHAPTER 10 Case Study: Androgen Insensitivity Syndrome (continued) In the summer after her first year of college, Carolyn underwent surgery for vaginal reconstruction in a large hospital on the West Coast. The surgeon first made an incision in the shallow vaginal opening between Carolyn’s urethra and anus. Then, mucous membrane transplants from her labia were used to enlarge the vaginal opening. Strips of flesh were also removed from the insides of her thighs to line the vagina, in order to give the vagina depth. By the time Carolyn returned to campus in the fall to begin her sophomore year, she was completely healed. She was no longer afraid of rejection by prospective male partners because she believed that she was now a complete woman. Hormonal Variations Other anomalies in sexual differentiation are produced by exposure to hormones or hormonelike chemicals. For example, in one disorder, called adrenogenital syndrome, female and male embryos are exposed to high levels of androgens in the uterus. This exposure to androgens is caused by the drugs administered to the mothers to prevent a miscarriage or by a disorder of the adrenal glands, which causes androgens to build up in the fetus’s body. Typically, these conditions cause blood androgen levels to be elevated later in the pregnancy, after the internal genitalia have developed but before the external genitalia develop. This means that the internal genitalia develop normally. Because the affected female embryo has a chromosomal designation of 46, XX, she has ovaries and develops a vagina, uterus, and fallopian tubes. However, the high blood androgen levels have a disastrous impact on the formation of her external genitalia. The high levels of androgen masculinize the external genitalia of the female embryo, in extreme cases transforming the genital tubercle and urethrogenital folds into a penis and the labioscrotal swelling into a scrotum. The affected individual is born with the external appearance of a male baby, although the scrotum is empty, and is often raised as a boy. Keep in mind, however, that this individual has ovaries and female internal genitalia. Imagine what happens at puberty: Estrogen released from the ovaries causes the breasts to develop, and menstruation begins, with menstrual fluid oozing out of the urethral opening of the penis. This can be extremely upsetting and confusing for an individual who has been raised as a boy. Often, these individuals elect to remain males because they have a masculine gender identity and because high levels of androgens have masculinized their brains. Surgical removal of the ovaries, uterus, and breast tissue and androgen therapy permits these individuals to remain male. Other individuals elect to revert to their biological sex and undergo reconstructive surgery to create female external genitalia (Schnitzer & Donahoe, 2001; White, 2001). As a result of genetic variations or hormonal irregularities, some individuals are born with ambiguous genitalia, such as an enlarged clitoris or a penis with unclosed urethrogenital folds. Other individuals, as you have learned in this chapter, are born with internal or external genitalia that do not match their chromosomal sex. In both cases these individuals are referred to as intersexed, or pseudohermaphrodites. Typically, intersexed individuals have gonads that are congruent with their chromosomal designation (that is, individuals who are 46, XY have testes, and those who are 46, XX have ovaries). Androgen insensitivity syndrome and androgenital syndrome are the two most common causes associated with pseudohermaphrodism (Al-Agha, Thomsett, & Batch, 2001; Farkas & Chertin, 2001). wiL81028_10_c10_301-326.indd 308 7/10/13 12:32 PM Section 10.1 Sexual Differentiation CHAPTER 10 Sex Differences in the Brain It is important to keep in mind that men produce estrogen in their adrenal glands and testes and that women produce androgens, including testosterone, in both their adrenal glands and ovaries. Thus, estrogen is not found exclusively in females, and testosterone is not found exclusively in males. The difference between hormone levels in men and women is a matter of degree. Typically, women have between 100 and 400 picograms (10–12 grams) of estrogen per milliliter of blood, whereas men have less than 50 picograms per milliliter. Men have between 300 and 900 nanograms (10–19 grams) of testosterone per deciliter of blood, and women have much less than 100 nanograms per deciliter. The roles of androgens in women and estrogens in men are largely unknown, although androgens are believed to contribute to sex drive in women, as they do in men. Stephen Simpson/Getty Images It is also important to remember that sex differences can result from different experiences that boys and girls Photo 10.1 Boys are typically given toys (and men and women) have, given their gender roles. that require or enhance visuospatial skills, For example, boys are typically given toys that require whereas girls are typically given toys that or enhance visuospatial skills, whereas girls are typically require or enhance fine motor skills. given toys that require or enhance fine motor skills. Thus, a particular brain structure may be more active in boys than in girls, or vice versa, due to the effect of playtime activities, rather than due to biological influences. Keep in mind, then, that a strong environmental component may contribute to the observed male-female differences. Sex Differences in Brain Structure The gonadal hormones, testosterone and estrogen, have organizational effects on the development of the brain, producing permanent sex differences in brain structure and function. Many areas of the developing brain are directly affected by the action of estrogen and testosterone. Of frequent scientific interest is the biological difference in overall brain size: Men tend to have larger overall brain sizes while women tend to exhibit proportionately more gray matter concentrations (Luders, Gaser, Narr, & Toga, 2009). At birth, the brains of boys and girls are the same size, and they remain the same size until the age of 2 years. Then, boys’ brains grow faster until full adult brain size is reached at 6 years of age. Androgens have been implicated in this increased growth of the male brain. In addition to overall size differences, a number of individual brain structures show sex-based size differences. One striking difference between the brains of men and women is the size of the corpus callosum. Recall from Chapter 4 that the corpus callosum is a wide band of axons that permits communication between the two cerebral hemispheres. A number of studies have revealed that the corpus callosum is thicker in women than in men (Menzler et al., 2011). Although the reason for this difference is unknown, the thicker corpus callosum in women allows for more intercommunication between the two halves of the cerebrum (Clarke, McCann, & Zaidel, 1998). That is, women tend to use both sides of their brains for speech and spatial functions, whereas men use only one wiL81028_10_c10_301-326.indd 309 7/10/13 12:32 PM CHAPTER 10 Section 10.1 Sexual Differentiation hemisphere for each (Hiscock, Inch, Hawryluk, Lyon, & Perachio, 1999; Lambe, 1999; Shaywitz et al., 1995). The increased interconnectivity between the two cerebral hemispheres in women might explain why women show fewer and less severe neurological deficits following damage to one hemisphere (Majewska, 1996; McGlone, 1978). Research with rats and humans has demonstrated that androgens contribute to the increased asymmetry seen in the brains of males (Geschwind & Galaburda, 1985). The cerebral cortex in the right hemisphere is thicker in the male brains of rats and human fetuses than in female brains (Diamond, 1991; de Lacoste, Adesanya, & Woodward, 1990). Jane Stewart and Bryan Kolb (1988) have shown that androgens act on the developing brain by suppressing the growth of the left cerebral cortex. Investigators are still debating whether these structural differences can explain the differences in verbal and spatial abilities observed in men and women. For example, learning and language disabilities are more common in males than in females, which might result from the suppressive effect of androgens on the left hemisphere (Geschwind & Galaburda, 1985; Hier, 1979; Lambe, 1999; Whitehouse et al., 2012). Other sex differences involve enlargements in certain areas of the hypothalamus that regulate sexual behavior, presumably due to the influence of testosterone. The third interstitial nucleus of the hypothalamus, for example, is larger in men than in women (Allen, Hines, Shryne, & Gorski, 1989). These differences are so large that they are visible without a microscope (Breedlove, 1994). Interestingly, the third interstitial nucleus is smaller in homosexual men than in heterosexual men, although the biological basis for this difference in unknown (LeVay, 1991). The “For Further Thought” box discusses the evidence for a biological explanation of homosexuality. For Further Thought: Biological Explanations of Homosexuality According to twenty-first century studies, approximately 5 to 10% of the world’s population identify as homosexual (Mengel, 2011). Because most people are heterosexual, we have come to think that heterosexual behavior is biologically based, especially because it produces offspring. But if heterosexual behavior is controlled by biology, is it not possible that biology can also influence homosexual behavior? A number of investigators have produced evidence that suggests that biology can determine a person’s sexual orientation. The evidence for a biological basis for homosexual orientation comes from anatomical, genetic, and psyPhoto 10.2 Although there are many studies chological research. The earliest evidence came from that present correlations between particular anatomists. Reporting that the suprachiasmatic nucleus brain structures and homosexuality, none of is enlarged in homosexual men, Swaab and Hofman (1990) were the first to describe a difference between these studies can actually explain the cause of homosexuality. the brains of gay and straight men. Along those lines of determining whether or not brain size contributed to biological homosexuality, LeVay (1991) found a significant difference in the size of a specific brain structure (the third interstitial nucleus of the anterior hypothalamus) that is directly implicated in the Dynamic Graphics/Getty Images/Creatas/Thinkstock (continued) wiL81028_10_c10_301-326.indd 310 7/10/13 12:32 PM Section 10.1 Sexual Differentiation CHAPTER 10 For Further Thought: Biological Explanations of Homosexuality (continued) control of male sexual behavior. According to LeVay’s findings, this interstitial nucleus is two to three times larger in heterosexual men than in women or homosexual men. That is, LeVay has demonstrated that a gay man has the interstitial nucleus of a woman, which may affect his sexual behavior. Although LeVay is a highly regarded scientist who conducted this study following stringent research protocols, a number of criticisms have been levied against his research. For example, LeVay’s findings assume that all people are exclusively homosexual or exclusively heterosexual and hence do not reflect the gradations of sexual activity that fall in between those two extremes. This hypothesis presumes that sexuality is fixed, while some researchers believe that sexual orientation and differentiation may develop over a person’s lifetime (Jannini, Blanchard, Camperio-Ciani, & Bancroft, 2010). In addition, all of LeVay’s homosexual subjects died of AIDS, which suggests that AIDS can affect the size of the third interstitial nucleus. However, six of the heterosexual men in LeVay’s study also died of AIDS, but their interstitial nuclei were all twice as large as those of gay men. Admittedly, there was wide variation in the size of the nuclei studied by LeVay, with much overlap between homosexual and heterosexual men. LeVay’s early studies might best be considered part of the scientific process of examining biology’s possible role in homosexual orientation, though ultimately much of his research is now outdated. In later cases, the difference between the size of the interstitial nucleus in gay and straight men was negligible (Fausto-Sterling, 1992). Another line of research that seeks to examine the possibility of a biological basis for homosexuality involves genetic studies. Early studies of twins have demonstrated that identical twins are twice as likely to both be gay than are fraternal twins and five times more likely to both be gay than adopted brothers are (Bailer & Pillard, 1991). Dean Hamer and his colleagues at the National Institutes of Health (NIH) located a region on the X chromosome, at position q28, that is shared by gay brothers but is not shared by heterosexual brothers (Hamer, Hu, Magnuson, Hu, & Pattatucci, 1993). A study by Stacey Cherny and her colleagues (Hu et al., 1995) supported Hamer’s findings by demonstrating that homosexual brothers, but not their heterosexual brothers, were likely to share the q28 marker on the X chromosome. However, Cherny’s group did not find shared Xq28 markers for lesbian sisters. Hamer’s research has come under attack by some investigators (Fausto-Sterling & Balaban, 1993; Rice, Anderson, Risch, & Ebers, 1999), but new studies suggest that while these markers do appear over the 50% mark, evidence for other linkages along chromosomes 7, 8, and 10 also exist (Jannini, Blanchard, Camperio-Ciani, & Bancroft, 2010; Dawood et al., 2009). In addition, genetic studies of “fruitless” fruit flies by Angela Pattatucci and Dean Hamer (1995) at NIH have also supported the notion that homosexuality has a genetic basis. The fruitless mutant is a male fruit fly that has functional sperm and sex organs but does not mate with females. Instead, this fruitless male is attracted to other males and, when in the presence of another male, will scurry around to the back end of the other and lick its genitals—behavior that is very unusual for normal fruit flies. Certainly human sexual behavior is more complicated than that of a fruit fly, but there is convincing evidence that some gene causes “fruitless” male fruit flies to engage in this atypical behavior and, at the same time, to avoid mounting and inseminating females. Psychological studies have also demonstrated biological differences between homosexual and heterosexual people. Dennis McFadden and Edward Pasanen (1999) at the University of Texas in Austin measured tiny echoes (called otoacoustic emissions) produced by the inner ears of 237 college-aged people. Typically, the inner ears of women produce much stronger echoes than those of men. However, McFadden and Pasanen found that lesbian and bisexual women produced significantly weaker (continued) wiL81028_10_c10_301-326.indd 311 7/10/13 12:33 PM Section 10.1 Sexual Differentiation CHAPTER 10 For Further Thought: Biological Explanations of Homosexuality (continued) echoes than strictly heterosexual women, whereas there was no difference between homosexual and straight men. Cheryl McCormick and Sandra Witelson at McMaster University in Canada have also studied biological differences between homosexual and heterosexual individuals. For example, they have found that gay men and lesbians are more likely than are heterosexual men and women to show a left-hand preference for many tasks (McCormick, Witelson, & Kingstone, 1990; McCormick & Witelson, 1991). Hand dominance and sexual orientation remain an object of study, and there are still cases that confirm a higher likelihood of left-handedness among homosexual males than heterosexual males (Brewster, Mullin, Dobrin, & Steeves, 2010). It is important to remember for all of these studies that correlation does not prove causation. That is, the fact that a particular gene is found only in gay men or that a particular brain structure is bigger or smaller in homosexual individuals does not mean that gene or that brain structure causes homosexual behavior. The scientific discussion about the role of biology in homosexual orientation remains in debate as studies attempt to be more objective in their methods and analysis (Jannini, Blanchard, Camperio-Ciani, & Bancroft, 2010). Sex Differences in Brain Activity PET scan studies have demonstrated differences in brain activity between men and women (Majewska, 1996). For example, women have 15% greater cerebral cortical blood flow than men do and significantly greater global (or overall) glucose metabolism (Gur & Gur, 1990). PET studies have also revealed that women have higher activity levels in the cingulate gyrus, whereas men have higher activity levels in the temporal lobe, limbic system, and cerebellum (Gur et al., Pam McLean/Purestock/SuperStock 1995). In some cases these differences mirror gender differences in Photo 10.3 Most males learn routes faster and with fewer ability or behavior. For example, errors than females, although females can recall more landmen and boys learn routes faster marks along the route. and with fewer errors than women and girls, although women and girls can recall more landmarks along the route (Galea & Kimura, 1993; Gibbs & Wilson, 1999). A functional MRI study in Germany at the University of Ulm indicated that different parts of the brain are activated when men and women learn a route (Gron, Wunderlich, Spitzer, Tomczak, & Riepe, 2000). The right side of the cerebrum concerned with spatial relationships and landmarks is activated when women learn a route. In contrast, the left prefrontal cortex and left hippocampus are activated when men learn a route. This sex difference may explain the differences in the ways men and women learn to navigate space although more current studies question whether or not gender differences may be eliminated from the debate (Chen, Chang, & Chang, 2009). wiL81028_10_c10_301-326.indd 312 7/10/13 12:33 PM Section 10.2 Regulation of Female Sexual Behavior CHAPTER 10 10.2 Regulation of Female Sexual Behavior E ggs, or ova, are produced by the ovaries in female animals, whereas sperm are produced by the testes in male animals (ova means “eggs” in Latin; ovum is the singular form of ova). The term “sexual behavior” refers to the behavior in which animals engage to bring eggs and sperm together. For aquatic animals, sexual behavior involves the female laying eggs and the male of the same species spraying the eggs with sperm. Sexual behavior in land-dwelling animals requires that the male deposit sperm into the genital tract of the female. Typically, female insects mate once during their lifetime, during which time they receive all the sperm they need from the males of the species. Most land-dwelling animals mate during a breeding season, when food and climate are optimal. Humans, like several other species, including dogs, cats, and rats, engage in sexual behavior year-round, regardless of the season. Sexual behavior is one aspect of reproductive behavior. Reproductive behavior involves producing children and nurturing them until they are able to live on their own. Thus, reproductive behavior consists of sexual behavior (bringing egg and sperm together) and parenting behavior (nurturing offspring). For most species, both sexual and parenting behaviors are driven by hormones. Let’s talk about hormones. As we begin this discussion, you will need to keep in mind two concepts: gonadal hormones and gonadotrophic hormones. Gonadal hormones are hormones that are produced by the gonads. For example, estrogen is a gonadal hormone that is produced in the ovaries, and testosterone is a gonadal hormone that is produced in the testes. In contrast, gonadotrophic hormones are hormones that are secreted by the pituitary gland and affect the gonads. Let’s examine how hormones regulate the sexual behavior of most mammalian species. We’ll start by looking at how hormones control female sexual behavior. In most species the female determines when mating, or sexual behavior, will occur. Her receptivity, or willingness to accept a male for sexual purposes, is determined by her hormonal status. The female animal experiences a series of hormonal fluctuations that is associated with the production and availability of ova for fertilization by sperm. These hormonal fluctuations are periodic and involve an interplay between gonadotrophic and gonadal hormones. The term ovarian cycle refers to the rhythmic fluctuations in the release of ovarian hormones, which produce a number of changes in the female’s body and in her behavior. At the beginning of the ovarian cycle, the hypothalamus directs the pituitary gland to begin the cycle. In response to the hypothalamus, the pituitary gland releases a gonadotrophic hormone called follicle-stimulating hormone (FSH). FSH travels in the bloodstream to the ovary, where it stimulates the maturation of one or more eggs. Each immature egg is stored in its own sac or follicle, and FSH causes one or more eggs to grow and mature. In addition, FSH also stimulates the ovary to produce the gonadal hormone, estrogen. Thus, FSH has two roles: It stimulates the maturation of one or more eggs, and it stimulates the production of estrogen. Estrogen is released into the bloodstream, where it travels to the brain and binds with estrogen receptors in the hypothalamus. Over time, under the influence of FSH, the ovary continues to pump out estrogen, and estrogen levels in the blood increase. When estrogen levels rise to a certain level, neurons in the hypothalamus send a message to the pituitary gland to stop the production of FSH and to begin the production of another gonadotrophic hormone called luteinizing hormone (LH). LH is transported in the bloodstream to the ovary, where it has a number of effects. wiL81028_10_c10_301-326.indd 313 7/10/13 12:33 PM CHAPTER 10 Section 10.2 Regulation of Female Sexual Behavior First, LH causes the mature egg to burst out of its follicle in a process called ovulation. The egg (ovum) is drawn into the fallopian tubes, which are located at the ends of the horns of the uterus, and it drifts down into the uterus. After the egg has been released from the ovaries, it is ready for fertilization by sperm, should sperm be present in the female’s genital tract. The fertilized egg then implants in the lining of the uterus, although sometimes it implants in the fallopian tubes or outside of the uterus, producing a tubal or ectopic pregnancy, which is lethal for the embryo (Figure 10.2). Figure 10.2: The human female reproductive system The ovaries are suspended by ligaments from the uterus (Figure A). An ectopic or tubal pregnancy occurs when the fertilized ovum implants in the wall of a fallopian tube (Figure B). A. Uterus Fallopian tube Ovary Vagina B. wiL81028_10_c10_301-326.indd 314 Ectopic pregnancy 7/10/13 12:33 PM Section 10.2 Regulation of Female Sexual Behavior CHAPTER 10 After the egg has erupted from the follicle, LH stimulates the ruptured follicle to become a corpus luteum. Under stimulation by LH, the corpus luteum produces two gonadal hormones: estrogen and progesterone. The purpose of progesterone is to prepare the body for pregnancy. For example, progesterone causes the uterine wall to thicken in preparation for pregnancy. As long as the pituitary gland continues to secrete LH, the corpus luteum stays intact and produces estrogen and progesterone. If the egg is fertilized by a sperm cell, pregnancy ensues. After the fertilized egg implants in the lining of the uterus, a specialized network of blood vessels, called a placenta, develops between the fertilized egg and uterine wall (Photo 10.4). Hormones released by the placenta trigger the continued release of LH, which stimulates the corpus luteum to produce progesterone and estrogen. As the pregnancy continues, the levels of estrogen and progesterone in the blood increase. The graph in Figure 10.3 illustrates the fluctuations in the levels of gonadal hormones through the ovarian cycle and throughout pregnancy. Note that ovulation takes place in the middle of the cycle. At ovulation, the female has one or Biophoto Associates/Science Source more eggs available for fertilization. These eggs (ova) can survive for up Photo 10.4 The placenta is a specialized network of blood vesto 72 hours, but they wither away sels that provide oxygen and nutrients to the developing fetus. if they are not fertilized during this period. If no sperm is available to fertilize the eggs, pregnancy does not occur, and no placenta is formed. This means that, during ovarian cycles that do not result in pregnancy, the eggs degenerate, and no placental hormones are produced. In the absence of placental hormones, the pituitary gland stops producing LH, which causes the corpus luteum in the ovary to wither away, too. As the corpus luteum degenerates, it stops producing progesterone and estrogen, causing the levels of both of these gonadal hormones to plummet. This drop in gonadal hormones signals the end of the ovarian cycle. In humans the drop in estrogen and progesterone levels causes the uterus to shed its inner lining, which was thickened by the rise in progesterone. When the uterus sheds its lining, it produces a bloody discharge that is released through the vagina, in a process called menstruation. During the period of time just before menstruation, which is called the premenstrual period, estrogen and progesterone levels are at their lowest (Figure 10.3). Lowered levels of serotonin, which produces insomnia and changes in mood, are associated with this premenstrual period in women. wiL81028_10_c10_301-326.indd 315 7/10/13 12:33 PM CHAPTER 10 Section 10.2 Regulation of Female Sexual Behavior You might be wondering how the cycle starts up again. As you’ve already learned, when estrogen levels rise, the hypothalamus directs the pituitary to stop producing FSH. However, after a pregnancy or during the premenstrual cycle, estrogen levels fall precipitously, prompting the hypothalamus to initiate FSH release by the pituitary gland. Thus, the ovarian cycle begins again when estrogen levels fall to some threshold level. The graph in Figure 10.3 depicts a 28-day ovarian cycle for women. In fact, the ovarian cycle varies among women, although most women have ovarian cycles that range from 12 to 55 days. Oral contraceptives, or birth control pills, prevent ovulation by tricking the hypothalamus. These pills contain a synthetic estrogen. When a woman swallows one oral contraceptive pill, the synthetic estrogen is sufficient to turns off the production of FSH. That is, as long as a woman takes a pill each day, estrogen levels in her blood remain high, which suppresses the release of FSH and prevents a new cycle from starting. However, if a woman forgets to take a pill, her estrogen levels fall, which could trigger the release of FSH and cause an egg to begin maturing in its follicle. When a woman completes taking all the pills in the 21-day cycle, the estrogen levels in her blood plummet, and the premenstrual period begins, producing menstruation within a day or two. Following menstruation, the woman who is trying to avoid pregnancy begins taking the contraceptive pills again, one a day, to prevent the release of FSH from the pituitary gland. Figure 10.3: Estrogen and progesterone levels throughout the ovarian cycle When estrogen levels reach a peak, luteinizing hormone is released, stimulating ovulation. Following ovulation, a corpus luteum is formed, and progesterone is released. Ovulation Estrogen Progesterone Luteinizing hormone 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 Days Sexual Receptivity in the Female Ovulation is usually associated with sexual receptivity in the females of most species, including primates (Adams, Gold, & Burt, 1978; Etgen, Chu, Fiber, Karkanias, & Morales, 1999; Slob, Bax, Hop, Rowland, & van der Werff ten Bosch 1996). Typically, in the period just before and during ovulation, nonhuman female animals change their behavior in ways that signal to males of their species that they are ready to mate. Many female animals release pheromones from glands in their genital tracts, which also communicate to the male that the female is sexually receptive. The term estrus refers to this period when a female is sexually receptive or “in heat.” wiL81028_10_c10_301-326.indd 316 7/10/13 12:33 PM Section 10.2 Regulation of Female Sexual Behavior CHAPTER 10 For example, a female rat is normally a shy and retiring animal that prefers to keep to herself. However, when she is in estrus, she can become quite fearless and aggressive, presenting herself to males for mating. If a male tries to copulate with her when she is not in estrus, the female rat will roll over on her back and will kick, squeal, and bite at the male. However, when she is in estrus and has mature eggs available for fertilization, she will permit the male to mount her sexually and will assume a position, called lordosis, in which her hindquarters are lifted slightly to make intromission of the penis easier for the male (Pfaff, Frohlich, & Morgan, 1968). On the other hand, the females of most primate species are sexually receptive and will copulate with males throughout the ovarian cycle. In some species sexual receptivity and copulation are used to communicate affection or high emotion. Bonobo monkeys, for example, copulate with friends, newcomers, and family members to communicate a welcome or greeting. Field studies have described incidents in which a female ape will present sexually to a male of the same species to avoid a beating or to gain a favor, such as a banana. All of this probably makes you wonder about human sexual behavior because female humans are sexually receptive throughout their ovarian cycles and even when they are pregnant. This state of perpetual sexual receptivity in women might be an evolutionary adaptation to keep the males of the species (that is, men) around for protection and to help provide food for their offspring. Although women engage in sexual activity throughout their ovarian cycle, masturbation and female-initiated sexual behavior occur with a significantly higher frequency at the time of ovulation. Adams et al. (1978) asked female participants to complete detailed daily questionnaires describing their sexual activity and found that female-initiated sexual behavior increased at ovulation for women who did not use oral contraception. Women who used oral contraception did not show an increase in sexual behavior at the time of ovulation because oral contraceptives suppress hormonal activity associated with ovulation. Similarly, women show greater sexual arousal and increased sexual activity around the time of ovulation. Studies have shown that in addition to increased sexual interest around ovulation, women’s interests often shift, including attraction to males who appear to be sexually unfaithful (Gangestad, Thornhill, & Garver-Apgar, 2010). Sex drive and sexual receptivity are observed in women who have had their ovaries surgically removed and in women who have gone through menopause, an aging process in which the ovaries stop functioning and cease their production of hormones. Thus, sex drive and sexual receptivity are not dependent on female gonadal hormones. In women, sex drive appears to be associated with the release of androgens by the adrenal glands and ovaries because drugs that increase androgen levels have been shown to increase sex drive in women (Rissman, 1995; et al., 2000). On the other hand, the female gonadal hormones estrogen and progesterone do appear to play a role in the regulation of mood in women (Janowsky, Halbreich, & Rausch, 1996), as you will learn in Chapter 12. Sexual Disorders in Women Sexual disorders in women fall into three general categories: disorders related to the ovarian cycle, fertility disorders, and disorders involving sexual response. wiL81028_10_c10_301-326.indd 317 7/10/13 12:33 PM Section 10.2 Regulation of Female Sexual Behavior CHAPTER 10 Amenorrhea Amenorrhea, or the absence of menstrual cycles, has two forms: primary amenorrhea and secondary amenorrhea. In primary amenorrhea the ovarian cycles never begin, although the young woman often shows signs of puberty onset. In secondary amenorrhea menstruation ceases prematurely, as when a woman develops the eating disorder anorexia nervosa. Both types of amenorrhea can be caused by a dysfunction of the ovaries or pituitary gland, which would interfere with the production of gonadal or gonadotrophic hormones. Developmental or genetic disorders, such as Turner’s syndrome or androgen insensitivity disorder, result in primary amenorrhea due to sterile or absent ovaries. Infertility Infertility is a condition in which the woman cannot conceive and get pregnant. Obviously, a woman without ovaries cannot get pregnant, nor can a woman who has had a hysterectomy, or surgery in which the uterus is removed (hyster- means “uterus” and -ectomy means “to remove” in Latin). However, infertility can also be caused by hormonal dysfunction, as when a woman does not produce FSH or progesterone. This condition can often be corrected with hormone replacement therapy. Some women have blocked fallopian tubes as a result of scarring or excessive growth of the endometrium, which lines the uterus. Although women with blocked fallopian tubes have regular ovarian cycles, the eggs cannot get into the uterus, and sperm cannot reach the eggs for fertilization. In vitro fertilization is the treatment of choice for blocked fallopian tubes. Eggs and sperm are mixed together on the lab bench, and fertilization takes place in a test tube. The fertilized eggs are then placed in the woman’s uterus for implantation. Typically, more than one fertilized egg is transferred to the uterus because the failure rate is quite high with this procedure, and most fertilized eggs do not survive. Dysmenorrhea Dysmenorrhea, or painful menstruation, occurs in about 25% of all women younger than age 25. Younger women usually experience spasmodic dysmenorrhea, which begins at the onset of menstruation and is characterized by severe cramping and abdominal pain. Congestive dysmenorrhea occurs primarily in older women. It occurs premenstrually and is experienced as abdominal pain and tenderness. Dysmenorrhea is usually treated with analgesics, or pain relievers, and hormones. Contraceptive pills are a ready source of estrogen and are often prescribed to reduce prostaglandin production, which is responsible for the pain of dysmenorrhea (Deligeoroglou, 2000). Loss of Sex Drive Some women suffer from a loss of sex drive, or loss of libido. A loss of libido may be associated with a decline in estrogen levels following hysterectomy or menopause, painful intercourse, depression, anxiety, or chronic stress (Graziottin, 2000). Typically, women with diminished wiL81028_10_c10_301-326.indd 318 Zen Shui/SuperStock Photo 10.5 Younger women usually experience spasmodic dysmenorrhea, which begins at the onset of menstruation and is characterized by severe cramping and abdominal pain. 7/10/13 12:33 PM Section 10.3 Regulation of Male Sexual Behavior CHAPTER 10 libido are not interested in engaging in sexual behavior, have reduced genital sensitivity, and are not aroused by stimuli that most women would find sexually exciting. Other women have difficulty achieving an orgasm. For most disorders involving loss of sex drive, effective treatment includes estrogen replacement therapy, androgen therapy (including testosterone treatment), and psychotherapy (Berman, Adhikari, & Goldstein, 2000; Sarrel, 2000; Shifren et al., 2000). Testosterone is used to treat impaired sexual arousal in women and produces an increase in sexual fantasies, masturbation, and other sexual activity in women with reduced sexual desire (Davis, 2000; Shifren et al., 2000). 10.3 Regulation of Male Sexual Behavior I n general, male animals can be divided in two groups: seasonal breeders and nonseasonal breeders. Seasonal breeders are those animals that mate only during a particular time of the year, typically when food supplies are abundant. In contrast, nonseasonal breeders are animals that mate throughout the year, regardless of the season or the availability of food. Most animals are seasonal breeders, although many species, such as humans, rats, dogs, and cats, are nonseasonal breeders. Since our focus is humans, we will examine nonseasonal breeders. Nonseasonal Breeders Nonseasonal breeders are sexually active throughout the year, regardless of season. They undergo a physical change called puberty, which involves sexual maturation. As puberty begins, the hypothalamus of the male nonseasonal breeder releases gonadotropin-releasing hormone to direct the pituitary gland to release FSH and interstitial cell-stimulating hormone or ICSH. Just like the seasonal breeder, FSH and ICSH cause sexual maturation. FSH stimulates the production of sperm cells in the testes, and ICSH stimulates the production of testosterone. Testosterone induces the growth of the penis and testes, as well as the development of secondary sex characteristics. Most importantly, testosterone binds with neurons in the hypothalamus, producing sex drive. However, unlike the seasonal breeder, the pituitary gland of the nonseasonal breeder continues to secrete FSH and ICSH continuously for the rest of the male’s life. Thus, the male nonseasonal breeder is always ready to copulate after puberty takes place. In the male human, secondary sex characteristics that arise during puberty include the growth of facial hair and hair on the legs, chest, armpits, and groin area. Testosterone also stimulates growth of the larynx, or voice box, which causes the voice to deepen, and it stimulates skeletal muscle development, as well as skeletal or bone growth (Figure 10.4). Because FSH and ICSH continue to be secreted until a man is well into his 80s, testosterone and sperm are produced in his testes until very late in life. This means that a man in his 70s or 80s still has a sex drive and is capable of impregnating a fertile woman. wiL81028_10_c10_301-326.indd 319 7/10/13 12:33 PM CHAPTER 10 Section 10.3 Regulation of Male Sexual Behavior Figure 10.4: Changes in the male human at puberty Many changes occur when a male experiences puberty. Postpuberty Puberty Prepuberty Hairline Facial hair Chin Voice (larynx) Axillary hair Body configuration Body hair Pubic hair Penis Length (cm) 3–8 4.5–9 4.5–12 8–15 9–15 10.5–18 Testes (cc) wiL81028_10_c10_301-326.indd 320 7/10/13 12:33 PM Section 10.3 Regulation of Male Sexual Behavior CHAPTER 10 Regulation of Sexual Behavior in Males Our understanding of how the male brain regulates sexual behavior is quite sophisticated. The medial preoptic area of the hypothalamus appears to be responsible for the expression of sexual behavior in males, because lesions of this area impair or eliminate sexual behavior in a wide variety of species (Van Furth, Wolterink, & Van Ree, 1995). The medial preoptic area receives input from many different areas of the brain, including the cerebral cortex, amygdala, septum, and midbrain. In general, opioids (whether endogenous opioids or administered drugs like heroin and morphine) have an inhibitory effect on the medial preoptic area and interfere with sexual performance (Argiolas, 1999). In contrast, dopamine has an excitatory effect on the medial preoptic area and facilitates sexual behavior in males. Release of dopamine from the nucleus accumbens results in increased sex drive and stimulates the medial preoptic area, producing sexual activity in males (Hull et al., 1999; Melis & Argiolas, 1995; Van Furth et al., 1995). Whereas dopamine excites sexual behavior, serotonin appears to inhibit it. Following ejaculation in the male, serotonin is released in the lateral hypothalamus and the medial preoptic area. This release of serotonin reduces sex drive by inhibiting the release of dopamine (Hull et al., 1999). Thus, dopamine promotes sexual arousal, and serotonin stimulates sexual satiation. For this reason, selective serotonin reuptake inhibitors (SSRIs), which increase serotonin activity, interfere with sexual arousal and orgasm. Both men and women who take an SSRI antidepressant can experience diminished genital sensitivity and a reduced ability to achieve orgasm. Sexual Disorders in Men Sexual disorders observed in men include fertility problems and sexual arousal dysfunction. Fertility problems include a low sperm count or sperm with low motility (that is, sperm that do not move as fast or as far as normal). Obviously, either of these problems can result in a failure to impregnate a woman. The causes for these disorders are unknown, but they have been associated with a number of factors, including heredity, chronic marijuana use, and wearing tight underwear that holds the testes close to the body. The scrotum that holds the testes hangs from a man’s body because sperm cells require storage in a temperature that is lower than core body temperature. Sperm cells are less viable when they are exposed to temperatures close to core body temperature. High temperatures associated with saunas, sitting with a laptop across your lap, and sitting for long periods in general may increase the temperature in testes, affecting sperm production (Mayo Clinic, 2012). Sexual arousal in men causes erection of the penis, which allows for intromission of the penis into a woman’s vagina and permits sperm to be deposited into her vaginal canal. Erection of the penis is caused by the relaxation of smooth muscles at the base of the penis. When relaxed, these muscles press against the veins that drain blood from the penis, resulting in a pooling of blood in the spongy tissues of the penis (Figure 10.5). To initiate an erection, conscious or unconscious signals from the cerebral cortex or limbic system are relayed to the hypothalamus. In turn, the hypothalamus stimulates the parasympathetic nervous system, causing acetylcholine to be released in the base of the penis. Acetylcholine induces the release of nitric oxide, which causes relaxation of the smooth muscles and, consequently, erection of the penis. Norepinephrine, released by the sympathetic nervous system, interferes with this process, by inducing contraction of the smooth muscles at the base of the penis. Thus, cold temperatures, anxiety, or fear, which stimulates the activity of the sympathetic nervous system, causes norepinephrine to be released in a man’s body, resulting in temporary shrinkage of the penis. wiL81028_10_c10_301-326.indd 321 7/10/13 12:33 PM CHAPTER 10 Section 10.3 Regulation of Male Sexual Behavior Figure 10.5: Control of penile erection In order for penile erection to occur, smooth muscles at the base of the penis press against veins that drain the penis, causing blood to pool in the spongy tissue of the penis. A. Male pelvis: side view C. Sequence leading to erection of the penis Ureter Bladder Sensory stimulation from periphery Thoughts, fantasies from cerebrum Rectum Pubic bone Hypothalamus Seminal vesicle Penile shaft Vas deferens Urethra Epididymus Glans penis Stimulation of the parasympathetic system Testis Scrotum B. Penile erection: blood pools in spongy tissue of the penis, as smooth muscles at the base of the penis press against the veins that drain the penis. Acetylcholine released in base of penis Nitric oxide released in base of penis Erection (reversible) Relaxation of smooth muscle in base of penis Erection About 10% of the male population experiences erectile dysfunction, due to nerve damage, hormonal disorders, alcoholism, cigarette smoking, or cardiovascular problems, such as high blood pressure and hardening of the arteries, that cause decreased blood flow to the penis (Melman & Christ, 2001). Approximately 20% of men with erectile dysfunction have significantly lower levels of testosterone in the blood than normal (Nehra, 2000). A number of treatments have been tried to treat erectile dysfunction disorder, including semirigid and inflatable penile implants, vacuum pumps, hormone treatments, and injections of muscle relaxants into the penis. Currently, the drug sildenafil (better known by its brand name, Viagra) is considered the most effective treatment for erectile dysfunction disorders. wiL81028_10_c10_301-326.indd 322 7/10/13 12:34 PM Section 10.4 Chapter Summary CHAPTER 10 Viagra triggers an erection by blocking an enzyme that breaks down cGMP, a molecule activated by nitric oxide to relax smooth muscles (Melman & Christ, 2001). That is, Viagra’s chief effect is to increase the availability of cGMP in smooth muscles in the penis, causing relaxation of those muscles and thus penile erection. However, Viagra is effective only in the presence of nitric oxide, which is released in response to sexual stimulation. If a man is not sexually aroused, Viagra does not stimulate penile erection. In Chapter 11 we will examine the role of neurotransmitters in the regulation of emotions. The hypothalamus and basal ganglia, which stimulate and coordinate sexual behavior, also play an important role in emotional behavior, as do other structures, including the limbic system and the prefrontal cortex. Many of the same chemicals and brain mechanisms are involved in both the regulation of sexual behavior and the regulation of emotion. 10.4 Chapter Summary • • • • • • • • • • • wiL81028_10_c10_301-326.indd 323 Sexual Differentiation The process by which we become biological males or females is called sexual differentiation. Sexual differentiation, which begins at conception, is largely determined by the chromosomes carried by the egg and the sperm to the fertilized egg. Normally, a biological female has two X chromosomes, whereas a biological male has one X and one Y chromosome. The Y chromosome directs the development of the testes, which produces two hormones, testosterone and Mullerian inhibiting substance. Testosterone affects the development of the internal and external genitalia, stimulating the growth of the Wolffian ducts and the penis and scrotum. Mullerian inhibiting substance prevents the growth of the Mullerian ducts, which normally develop into female internal genitalia. The presence or absence of male gonadal hormones affects the development of internal and external genitalia. In the absence of a Y chromosome, the ovaries develop, and female internal and external genitalia develop. Individuals with Turner’s syndrome have a chromosomal designation of 45, XO and are typically raised as girls. Individuals with Klinefelter’s syndrome have a chromosomal designation of 47, XXY, possess testes, and are raised as boys. Androgen insensitivity syndrome occurs in individuals with a chromosomal designation of 46, XY, who are born with testes but are insensitive to testosterone. In adrenogenital syndrome, embryos are exposed to high levels of androgens, which masculinize the external genitalia of female embryos. The brain is also influenced by sexual differentiation, which alters brain structures and activity. The corpus callosum is larger in women than in men. In contrast, the interstitial nucleus of the hypothalamus is larger in men than in women. Male sex hormones, called androgens, appear to suppress the growth of the left cerebral cortex, causing the right cortex to be thicker than the left cortex in male rats and humans. Hormonal Regulation of Female Sexual Behavior Gonadal hormones are hormones produced by the ovaries or testes. Gonadotrophic hormones are hormones produced by the pituitary gland that stimulate changes in the gonads. Sexual behaviors in nonhuman animals are regulated by hormonal activity, and some human sexual behavior has been linked to gonadal hormones as well. 7/10/13 12:34 PM Web Links • • • • • • • CHAPTER 10 In female animals ovulation is produced by an interplay of pituitary (FSH, LH) and gonadal (estrogen, progesterone) hormones. Follicle-stimulating hormone (FSH) causes maturation of immature eggs in the ovary, and luteinizing hormone (LH) is released by the pituitary when estrogen levels reach an optimum level, causing ovulation. Amenorrhea refers to the absence of menstrual cycles, which can be caused by hormonal, genetic, or developmental disorders. Infertility is a condition in which a woman cannot conceive and get pregnant. Painful menstruation, called dysmenorrhea, occurs in about one fourth of all women younger than age 25. Hormonal Regulation of Male Sexual Behavior Male animals are classified as seasonal or nonseasonal breeders. Nonseasonal breeders undergo a physical change, called puberty, which brings about sexual maturation. At puberty, FSH and ICSH are released by the pituitary gland, stimulating the production of sperm and testosterone. Sexual disorders in men include fertility problems and erectile dysfunction. The medial preoptic area of the hypothalamus regulates sexual behavior in male animals. Dopamine stimulates sexual behaviors in males, whereas serotonin inhibits it. Questions for Thought 1. 2. 3. 4. What does it mean to be male? What does it mean to be female? Can autosomes play a role in sexual differentiation? Explain. What is the relationship between the hypothalamus and the pituitary gland? What causes the Wolffian system to develop? What causes the Mullerian system to develop? 5. What role do pituitary hormones play in the female ovarian cycle? 6. What role do pituitary hormones play in male sexual behavior? 7. How do dopamine and serotonin affect sexual behavior? Web Links The American Psychological Association’s website provides a brief summary of sexual orientation, the definitions of gay and lesbian, and resources to learn more about homosexuality. http://www.apa.org Visit the Intersex Society of North America’s website to learn more about intersex individuals and how the organization is helping to end the shame, secrecy, and unwanted genital surgeries for people born with atypical reproductive anatomies. http://www.isna.org wiL81028_10_c10_301-326.indd 324 7/10/13 12:34 PM CHAPTER 10 Key Terms Key Terms adrenogenital syndrome A disorder in which embryos are exposed to high levels of androgens in the uterus, which masculinizes the female embryo. menstruation A process in the human female body in which the uterus sheds its lining, producing a bloody discharge, when estrogen and progesterone levels fall. amenorrhea The absence of menstrual cycles. Mullerian inhibiting substance A hormone secreted by the testes that inhibits the development of the Mullerian ducts, which means that the vagina, uterus, and fallopian tubes do not develop in the male body. androgen insensitivity syndrome A disorder in which the affected individual is insensitive to all androgens, including testosterone. corpus luteum A yellowish structure in the ovary, which was formerly a ruptured follicle, that produces progesterone. dihydrotestosterone The androgen that converts the embryonic external genitalia into the penis and scrotum. dysmenorrhea A condition in which a woman experiences painful menstruation. estrogen A gonadal hormone produced by the ovaries. estrus A time period during which a nonhuman female is sexually receptive. follicle-stimulating hormone (FSH) A gonadotrophic hormone that stimulates the maturation of immature egg and sperm. gonadal hormones Hormones produced by the male or female gonads. gonadotrophic hormones Hormones secreted by the pituitary gland that alter the function of the gonads. infertility A condition in which a woman cannot conceive and become pregnant. intersexed A condition in which a person has an atypical reproductive anatomy. nonseasonal breeders Animals that mate throughout the year, regardless of the season or the availability of food. ovary A female gonad. ovulation A process in which the mature ovum bursts out of the ovarian follicle and is available for fertilization. placenta A specialized network of blood vessels that provide oxygen and nutrients to the developing fetus. primordial gonads In embryonic development, the two undifferentiated gonads that are capable of taking a male or female form. progesterone A gonadal hormone produced by the ovaries that prepares the female body for pregnancy. puberty A physical change that involves sexual maturation and occurs in nonseasonal breeders. reproductive behavior The process of producing children and nurturing them until they are able to live on their own; it consists of sexual behavior (bringing egg and sperm together) and parenting behavior (nurturing offspring). Klinefelter’s syndrome A genetic disorder in which a person has an extra sex chromosome. seasonal breeders Animals that mate only during a particular time of the year, typically when food supplies are abundant. luteinizing hormone (LH) A gonadotrophic hormone that initiates ovulation and stimulates the development of the corpus luteum. sexual differentiation The process by which we become biological males or females. wiL81028_10_c10_301-326.indd 325 7/10/13 12:34 PM Key Terms testes Male gonads (singular is testis). testosterone A hormone produced by the male gonads or testes. true hermaphrodites Individuals born with both ovarian and testicular tissue. Turner’s syndrome A syndrome in which affected individuals have chromosomal designation of 45, XO, which results in the development of female internal and external genitalia and sterile ovaries. wiL81028_10_c10_301-326.indd 326 CHAPTER 10 Wolffian ducts The precursors of the male internal genitalia; under the influence of testosterone, they develop into the internal plumbing of the normal male reproductive system. X chromosome One of the two chromosomes (along with the Y chromosome) that determine sex; the ovum always carries an X chromosome, while the sperm can carry either an X or a Y chromosome. Y chromosome The tiny sex chromosome that directs the development of the testes. 7/10/13 12:34 PM 
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